Respiratory acidosis

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Respiratory acidosis
Davenport diagram
SpecialtyIntensive care medicine, pulmonology, internal medicine Edit this on Wikidata

Respiratory acidosis is a state in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis).

Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through

PaCO2 (a condition called hypercapnia
). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH.

Types

Respiratory acidosis can be acute or chronic.

Causes

Acute

Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the

amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy
), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Chronic

Chronic respiratory acidosis may be secondary to many disorders, including

diaphragm
function secondary to fatigue and hyperinflation.

Chronic respiratory acidosis also may be secondary to

thoracic
deformities.

Lung diseases that primarily cause abnormality in

alveolar gas exchange
usually do not cause hypoventilation but tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue occurs.

Physiological response

Mechanism

Metabolism rapidly generates a large quantity of volatile acid (H2CO3) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2. The CO2 combines with H2O to form carbonic acid (H2CO3). The lungs normally excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO2 can cause a respiratory acid-base disorder. The PaCO2 is maintained within a range of 35–45 mm Hg in normal states.

Alveolar ventilation is under the control of the

stretch receptors and impulses from the cerebral cortex
. Failure of ventilation quickly increases the PaCO2.

In acute respiratory acidosis, compensation occurs in 2 steps.

Estimated changes

In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in

PaCO2
. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:

  • Acute respiratory acidosis: HCO3− increases 1 mEq/L for each 10 mm Hg rise in PaCO2.
  • Chronic respiratory acidosis: HCO3− rises 3.5 mEq/L for each 10 mm Hg rise in PaCO2.

The expected change in pH with respiratory acidosis can be estimated with the following equations:

  • Acute respiratory acidosis: Change in pH = 0.08 X ((40 −
    PaCO2
    )/10)
  • Chronic respiratory acidosis: Change in pH = 0.03 X ((40 − PaCO2)/10)

Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia.

Diagnosis

Diagnoses can be done by doing an ABG (Arterial Blood Gas) laboratory study, with a pH <7.35 and a PaCO2 >45 mmHg in an acute setting. Patients with COPD and other Chronic respiratory diseases will sometimes display higher numbers of PaCO2 with HCO3- >30 and normal pH.

Terminology

  • Acidosis refers to disorders that lower cell/tissue pH to < 7.35.
  • Acidemia refers to an arterial pH < 7.36.[2]

See also

References

  1. ISBN 1-4160-2328-3
    .
  2. PMID 19932372
    .

External links
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